Dysregulation of Ca ²⁺ movement in platelets from patients with acute ischaemic stroke

Platelets play a pivotal role during acute ischaemic stroke. An increase in cytosolic Ca ²⁺ concentrations ([Ca ²⁺] _i) triggers intracellular signal transduction, leading to platelet aggregation and thrombosis. In the present study, we examined the differences between platelets from acute ischaemic stroke patients and at-risk controls in terms of the increase in platelet [Ca ²⁺] _i. Thirty-one patients with acute ischaemic stroke and 27 at-risk controls were enrolled in the present study. Platelet [Ca ²⁺] _i was measured using the fluorescent dye fura-2 after stimulation with 100 μmol/L arachidonic acid (AA), 10 μmol/L ADP, 1 μmol/L platelet-activation factor (PAF) and 0.1 U/mL thrombin. Basal [Ca ²⁺] _i was higher in the stroke group compared with at-risk controls, irrespective of the presence or absence of extracellular Ca ²⁺. In Ca ²⁺-containing medium, both PAF and ADP, but not AA and thrombin, significantly increased platelet [Ca ²⁺] _i in the stroke group compared with the at-risk controls. However, in Ca ²⁺-free medium, only PAF significantly increased platelet [Ca ²⁺] _i in the stroke group compared with the at-risk controls. Basal [Ca ²⁺] _i and PAF-induced platelet [Ca ²⁺] _i increases were still higher in the stroke group at the subacute stage than in the at-risk controls. The results of the present study provide direct evidence that Ca ²⁺ signalling in platelets from acute ischaemic stroke patients was altered in response to particular stimuli. The dysregulation of Ca ²⁺ movement in platelets may persist up to the subacute stage of ischaemic stroke.